Department of Anesthesiology and Critical Care Medicine, Yokohama City University Graduate School of Medicine, Yokohama, Kanagawa, Japan.
Department of Pathology, Dokkyo Medical University, Tochigi, Japan.
Crit Care. 2018 Sep 23;22(1):228. doi: 10.1186/s13054-018-2154-2.
The open lung approach (OLA) reportedly has lung-protective effects against acute respiratory distress syndrome (ARDS). Recently, lowering of the driving pressure (ΔP), rather than improvement in lung aeration per se, has come to be considered as the primary lung-protective mechanism of OLA. However, the driving pressure-independent protective effects of OLA have never been evaluated in experimental studies. We here evaluated whether OLA shows protective effects against experimental ARDS even when the ΔP is not lowered.
Lipopolysaccharide was intratracheally administered to rats to establish experimental ARDS. After 24 h, rats were mechanically ventilated and randomly allocated to the OLA or control group. In the OLA group, 5 cmHO positive end-expiratory pressure (PEEP) and recruitment maneuver (RM) were applied. Neither PEEP nor RM was applied to the rats in the control group. Dynamic ΔP was kept at 15 cmHO in both groups. After 6 h of mechanical ventilation, rats in both groups received RM to inflate reversible atelectasis of the lungs. Arterial blood gas analysis, lung computed tomography, histological evaluation, and comprehensive biochemical analysis were performed.
OLA significantly improved lung aeration, arterial oxygenation, and gas exchange. Even after RM in both groups, the differences in these parameters between the two groups persisted, indicating that the atelectasis-induced respiratory dysfunction observed in the control group is not an easily reversible functional problem. Lung histological damage was severe in the dorsal dependent area in both groups, but was attenuated by OLA. White blood cell counts, protein concentrations, and tissue injury markers in the broncho-alveolar lavage fluid (BALF) were higher in the control than in the OLA group. Furthermore, levels of CXCL-7, a platelet-derived chemokine, were higher in the BALF from the control group, indicating that OLA protects the lungs by suppressing platelet activation.
OLA shows protective effects against experimental ARDS, even when the ΔP is not decreased. In addition to reducing ΔP, maintaining lung aeration seems to be important for lung protection in ARDS.
据报道，开放肺策略（OLA）对急性呼吸窘迫综合征（ARDS）具有肺保护作用。最近，降低驱动压（ΔP）而不是改善肺充气本身被认为是 OLA 的主要肺保护机制。然而，OLA 的驱动压独立保护作用在实验研究中从未得到评估。我们在此评估了即使 ΔP 未降低，OLA 是否对实验性 ARDS 仍具有保护作用。
通过气管内给予脂多糖建立大鼠实验性 ARDS。24 小时后，大鼠进行机械通气，并随机分配到 OLA 或对照组。在 OLA 组，给予 5cmH 2 O 的呼气末正压（PEEP）和复张手法（RM）。对照组大鼠不给予 PEEP 或 RM。两组的动态 ΔP 均保持在 15cmH 2 O。机械通气 6 小时后，两组均给予 RM 以膨胀肺可复张性肺不张。进行动脉血气分析、肺计算机断层扫描、组织学评估和综合生化分析。
OLA 显著改善了肺充气、动脉氧合和气体交换。即使在两组均给予 RM 后，两组之间这些参数的差异仍然存在，这表明对照组中观察到的与肺不张相关的呼吸功能障碍不是一种容易逆转的功能问题。两组背侧依赖区的肺组织学损伤均严重，但 OLA 减轻了损伤。对照组支气管肺泡灌洗液（BALF）中的白细胞计数、蛋白浓度和组织损伤标志物较高。此外，对照组 BALF 中的趋化因子 CXCL-7 水平较高，表明 OLA 通过抑制血小板激活来保护肺。
OLA 对实验性 ARDS 具有保护作用，即使 ΔP 没有降低。除了降低 ΔP 外，维持肺充气对于 ARDS 的肺保护似乎也很重要。
